tbuckley/cabot-search huggingface dataset:
Abortion Surveillance: Preliminary Analysis--United States, 1995
Journal: JAMA (1998)

For 1996, CDC compiled data about legal induced abortions from the 50 states, New York City, and the District of Columbia. The total number of legal induced abortions was available from all reporting areas; however, not all areas collected information about the characteristics of women who obtained abortions. This report presents preliminary data for 1996; final abortion data for 1996 will be published during spring 1999.
Modified Biodegradation Behavior Induced Beneficial Microenvironments for Bone Regeneration by Low Addition of Gadolinium in Zinc
Authors: Hongtao Yang, Bo Jia, Xinhua Qu, Kerong Dai, Yufeng Zheng
Journal: Advanced Healthcare Materials (2022)

Zinc (Zn) shows a great potential as a biodegradable material for bone implants after a decade of systematic research and development. However, uncontrollable biodegradation behavior and biphasic dose-response prevent Zn from fulfilling its essential role in facilitating bone regeneration. In this study, the low addition of gadolinium (Gd) modifies the intrinsic microstructure of Zn in terms of grain size distribution, grain boundary misorientation, and texture. Adding Gd refines grain size distribution and creates a stronger basal plane texture in Zn, consequently, changing the current density distribution and reducing the anode dissolution rate during corrosion. As a result, uniform degradation is more predominant in Zn-0.4Gd alloy implant, in comparison to localized degradation in pure Zn implant in bone environments. The modified biodegradation behavior of the Zn-0.4Gd alloy implant induces significantly better new bone formation and osseointegration compared to the pure Zn implant. Therefore, Gd with trace amounts is able to tune the degradation behavior and improve the performance of Zn-based implants in promoting bone regeneration.
Knockdown of MicroRNA Let-7a Improves the Functionality of Bone Marrow-Derived Mesenchymal Stem Cells in Immunotherapy
Authors: Yang Yu, Li Liao, Bingyi Shao, Xiaoxia Su, Yi Shuai, Han Wang, Fengqing Shang, Zhifei Zhou, Deqin Yang, Yan Jin
Journal: Molecular Therapy (2022)

(Molecular Therapy 25, 480–493; February 2017) The authors of this article have reported that some images in Figures 3A, 3D, and 4E have been used in both this article and “Redundant let-7a suppresses the immunomodulatory properties of BMSCs by inhibiting the Fas/FasL system in osteoporosis” (https://doi.org/10.1096/fj.201700885R). An image in Figure 4E was also reused in Figure 6E within the Molecular Therapy article. FASEB is issuing a correction for “Redundant let-7a suppresses the immunomodulatory properties of BMSCs by inhibiting the Fas/FasL system in osteoporosis.” Molecular Therapy has requested all original data for “Knockdown of MicroRNA Let-7a Improves the Functionality of Bone Marrow-Derived Mesenchymal Stem Cells in Immunotherapy” for review. We are publishing this editorial expression of concern while the editors investigate the issues raised by the authors. Knockdown of MicroRNA Let-7a Improves the Functionality of Bone Marrow-Derived Mesenchymal Stem Cells in ImmunotherapyYu et al.Molecular TherapyDecember 11, 2016In BriefKnockdown of let-7a, a conservative miRNA targeting the 3′ UTR of both Fas and FasL mRNA, elevated Fas/FasL protein levels. The increased Fas induced T cell migration, while the increased FasL triggered T cell apoptosis, providing a potential strategy to improve MSC immunotherapy for inflammatory diseases in clinic. Full-Text PDF Open Archive
Glial control of sphingolipid levels sculpts diurnal remodeling in a circadian circuit
Authors: John P. Vaughen, Emma Theisen, Irma Magaly Rivas-Serna, Andrew B. Berger, Prateek Kalakuntla, Ina Anreiter, Vera C. Mazurak, Tamy Portillo Rodriguez, Joshua D. Mast, Tom Hartl, Ethan O. Perlstein, Richard J. Reimer, M. Thomas Clandinin, Thomas R. Clandinin
Journal: Neuron (2022)
Advisory Board and Contents
Authors: Jerry Madukwe, Danielle Loughlin, Fred Kop, Patrick Scheffmann, Michelle Arkin, Matthew Banks, Andrew Bate, Mary Bebawy, Jeffrey Benovic, Jacqueline Crawley, Debbie Hay, Stephanie Laszlo, Hunyady Magnus, Ingelman-Sundberg Michael, Kassiou Kum, Kum Khanna, Brian Kobilka, Jenny Lam, Michel Lazdunski, Fiona Marshall, Ruth Nussinov, Avner Schlessinger, Martina Schmidt, Harald Sitte, Rachel Tyndale, Ming-Wei Wang, Stephen Watson, Stephen Waxman, Matthew Webber, Mazharul Maishan, Diana Lim, Guy Zimmerman, Michael Matthay, Zak Whiting, Jiazhen Yin, Sara De La Harpe, Andrea Vernall, Natasha Grimsey, Jason Lynch, Lisa Goers, Cammie Lesser
Journal: Trends in Pharmacological Sciences (2022)
Harmonization of the American College of Cardiology/American Heart Association and European Society of Cardiology/European Society of Hypertension Blood Pressure/Hypertension Guidelines
Authors: Paul K. Whelton, Robert M. Carey, Giuseppe Mancia, Reinhold Kreutz, Joshua D. Bundy, Bryan Williams
Journal: Journal of the American College of Cardiology (2022)

The 2017 American College of Cardiology/American Heart Association and 2018 European Society of Cardiology/European Society of Hypertension clinical practice guidelines for management of high blood pressure/hypertension are influential documents. Both guidelines are comprehensive, were developed using rigorous processes, and underwent extensive peer review. The most notable difference between the 2 guidelines is the blood pressure cut points recommended for the diagnosis of hypertension. There are also differences in the timing and intensity of treatment, with the American College of Cardiology/American Heart Association guideline recommending a somewhat more intensive approach. Overall, there is substantial concordance in the recommendations provided by the 2 guideline-writing committees, with greater congruity between them than their predecessors. Additional harmonization of future guidelines would help to underscore the commonality of their core recommendations and could serve to catalyze changes in practice that would lead to improved prevention, awareness, treatment, and control of hypertension, worldwide.
CD248 Regulates Wnt Signaling in Pericytes to Promote Angiogenesis and Tumor Growth in Lung Cancer
Authors: Chia-Lun Hong, I-Shing Yu, Chen-Hsueh Pai, Jin-Shing Chen, Min-Shu Hsieh, Hua-Lin Wu, Shu-Wha Lin, Hsiang-Po Huang
Journal: Cancer Research (2022)

Abstract The tumor microenvironment plays a central role in cancer initiation and progression. CD248 is expressed in tumor-associated stromal cells, particularly fibroblasts and pericytes. Exploring the function of CD248 has the potential to provide biological insights into tumor-supportive stroma and potential therapeutic targets. Here, we investigated the role of stromal CD248 in lung cancer. In orthotopic lung cancer transplantation models, tumor volume, density of vessels and pericytes, and functionality of tumor vessels were all lower in mice lacking Cd248 (Cd248LacZ/LacZ) compared with Cd248 wild-type or haploinsufficient mice. Two angiogenic factors, OPN and SERPINE1, were decreased in Cd248LacZ/LacZ pericytes, and supplementation with both factors rescued their proliferation and endothelial cell tube formation–promoting ability. Mechanistically, Wnt/β-catenin signaling induced Opn and Serpine1 expression and was suppressed in Cd248LacZ/LacZ pericytes. CD248 interacted with Wnt pathway repressors IGFBP4 and LGALS3BP, leading to increased Wnt/β-catenin signaling. Correspondingly, administration of a β-catenin inhibitor in Cd248+/LacZ mice mimicked the effect of Cd248 loss and blocked the growth of transplanted lung tumor cells that were resistant to this inhibitor in vitro. In addition, CD248+ pericytes coexpressed OPN and SERPINE1 and correlated with increased tumor size in human lung cancer. Additionally, high expression of CD248, OPN, and SERPINE1 was associated with poor survival in lung cancer patients. In summary, CD248 derepresses Wnt signaling and upregulates OPN and SERPINE1 in pericytes, resulting in enhanced angiogenesis and lung cancer growth. This novel axis of CD248–Wnt signaling–angiogenic factors in pericytes provides a potential target for lung cancer therapy. Significance: These findings demonstrate that CD248 maintains pericyte function in lung cancer through the Wnt signaling pathway and present CD248 as a potential therapeutic target.
A Distinct Chromatin State Drives Therapeutic Resistance in Invasive Lobular Breast Cancer
Authors: Agostina Nardone, Xintao Qiu, Sandor Spisak, Zsuzsanna Nagy, Ariel Feiglin, Avery Feit, Gabriela Cohen Feit, Yingtian Xie, Alba Font-Tello, Cristina Guarducci, Francisco Hermida-Prado, Sudeepa Syamala, Klothilda Lim, Miguel Munoz Gomez, Matthew Pun, MacIntosh Cornwell, Weihan Liu, Aysegul Ors, Hisham Mohammed, Paloma Cejas, Jane B. Brock, Matthew L. Freedman, Eric P. Winer, Xiaoyong Fu, Rachel Schiff, Henry W. Long, Otto Metzger Filho, Rinath Jeselsohn
Journal: Cancer Research (2022)

Abstract Most invasive lobular breast cancers (ILC) are of the luminal A subtype and are strongly hormone receptor–positive. Yet, ILC is relatively resistant to tamoxifen and associated with inferior long-term outcomes compared with invasive ductal cancers (IDC). In this study, we sought to gain mechanistic insights into these clinical findings that are not explained by the genetic landscape of ILC and to identify strategies to improve patient outcomes. A comprehensive analysis of the epigenome of ILC in preclinical models and clinical samples showed that, compared with IDC, ILC harbored a distinct chromatin state linked to gained recruitment of FOXA1, a lineage-defining pioneer transcription factor. This resulted in an ILC-unique FOXA1–estrogen receptor (ER) axis that promoted the transcription of genes associated with tumor progression and poor outcomes. The ILC-unique FOXA1–ER axis led to retained ER chromatin binding after tamoxifen treatment, which facilitated tamoxifen resistance while remaining strongly dependent on ER signaling. Mechanistically, gained FOXA1 binding was associated with the autoinduction of FOXA1 in ILC through an ILC-unique FOXA1 binding site. Targeted silencing of this regulatory site resulted in the disruption of the feed-forward loop and growth inhibition in ILC. In summary, ILC is characterized by a unique chromatin state and FOXA1–ER axis that is associated with tumor progression, offering a novel mechanism of tamoxifen resistance. These results underscore the importance of conducting clinical trials dedicated to patients with ILC in order to optimize treatments in this breast cancer subtype. Significance: A unique FOXA1–ER axis in invasive lobular breast cancer promotes disease progression and tamoxifen resistance, highlighting a potential therapeutic avenue for clinical investigations dedicated to this disease. See related commentary by Blawski and Toska, p. 3668
Targeting Plk1 Sensitizes Pancreatic Cancer to Immune Checkpoint Therapy
Authors: Zhuangzhuang Zhang, Lijun Cheng, Jie Li, Qi Qiao, Anju Karki, Derek B. Allison, Nuha Shaker, Kunyu Li, Sagar M. Utturkar, Nadia M. Atallah Lanman, Xiongjian Rao, Piotr Rychahou, Daheng He, Stephen F. Konieczny, Chi Wang, Qing Shao, B. Mark Evers, Xiaoqi Liu
Journal: Cancer Research (2022)

Polo-like kinase 1 (Plk1) plays an important role in cell-cycle regulation. Recent work has suggested that Plk1 could be a biomarker of gemcitabine response in pancreatic ductal adenocarcinoma (PDAC). Although targeting Plk1 to treat PDAC has been attempted in clinical trials, the results were not promising, and the mechanisms of resistance to Plk1 inhibition is poorly understood. In addition, the role of Plk1 in PDAC progression requires further elucidation. Here, we showed that Plk1 was associated with poor outcomes in patients with PDAC. In an inducible transgenic mouse line with specific expression of Plk1 in the pancreas, Plk1 overexpression significantly inhibited caerulein-induced acute pancreatitis and delayed development of acinar-to-ductal metaplasia and pancreatic intraepithelial neoplasia. Bioinformatics analyses identified the regulatory networks in which Plk1 is involved in PDAC disease progression, including multiple inflammation-related pathways. Unexpectedly, inhibition or depletion of Plk1 resulted in upregulation of PD-L1 via activation of the NF-κB pathway. Mechanistically, Plk1-mediated phosphorylation of RB at S758 inhibited the translocation of NF-κB to nucleus, inactivating the pathway. Inhibition of Plk1 sensitized PDAC to immune checkpoint blockade therapy through activation of an antitumor immune response. Together, Plk1 suppresses PDAC progression and inhibits NF-κB activity, and targeting Plk1 can potentiate the efficacy of immunotherapy in PDAC.
A First-in-Class Inhibitor of ER Coregulator PELP1 Targets ER+ Breast Cancer
Authors: Kristin A. Altwegg, Suryavathi Viswanadhapalli, Monica Mann, Dimple Chakravarty, Samaya Krishnan, Zexuan Liu, Junhao Liu, Uday P. Pratap, Behnam Ebrahimi, John R. Sanchez, Xiaonan Li, Shihong Ma, Ben H. Park, Bindu Santhamma, Yidong Chen, Zhao Lai, Ganesh V. Raj, Yaxia Yuan, Daohong Zhou, Gangadhara R. Sareddy, Rajeshwar R. Tekmal, Stan McHardy, Tim H.-M. Huang, Manjeet K. Rao, Hariprasad Vankayalapati, Ratna K. Vadlamudi
Journal: Cancer Research (2022)

Abstract Most patients with estrogen receptor alpha–positive (ER+) breast cancers initially respond to treatment but eventually develop therapy resistance with disease progression. Overexpression of oncogenic ER coregulators, including proline, glutamic acid, and leucine-rich protein 1 (PELP1), are implicated in breast cancer progression. The lack of small molecules that inhibits PELP1 represents a major knowledge gap. Here, using a yeast-two-hybrid screen, we identified novel peptide inhibitors of PELP1 (PIP). Biochemical assays demonstrated that one of these peptides, PIP1, directly interacted with PELP1 to block PELP1 oncogenic functions. Computational modeling of PIP1 revealed key residues contributing to its activity and facilitated the development of a small-molecule inhibitor of PELP1, SMIP34, and further analyses confirmed that SMIP34 directly bound to PELP1. In breast cancer cells, SMIP34 reduced cell growth in a dose-dependent manner. SMIP34 inhibited proliferation of not only wild-type (WT) but also mutant (MT) ER+ and therapy-resistant breast cancer cells, in part by inducing PELP1 degradation via the proteasome pathway. RNA sequencing analyses showed that SMIP34 treatment altered the expression of genes associated with estrogen response, cell cycle, and apoptosis pathways. In cell line–derived and patient-derived xenografts of both WT and MT ER+ breast cancer models, SMIP34 reduced proliferation and significantly suppressed tumor progression. Collectively, these results demonstrate SMIP34 as a first-in-class inhibitor of oncogenic PELP1 signaling in advanced breast cancer. Significance: Development of a novel inhibitor of oncogenic PELP1 provides potential therapeutic avenues for treating therapy-resistant, advanced ER+ breast cancer.
The Clinical Study and Treatment of Sick Children.
Journal: JAMA (1926)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The 2022 World Health Organization Classification of Tumors of the Urinary System and Male Genital Organs—Part B: Prostate and Urinary Tract Tumors
Authors: George J Netto, Mahul B Amin, Daniel M Berney, Eva M Compérat, Anthony J Gill, Arndt Hartmann, Santosh Menon, Maria R Raspollini, Mark A Rubin, John R Srigley, Puay Hoon Tan, Satish K Tickoo, Toyonori Tsuzuki, Samra Turajlic, Ian Cree, Holger Moch
Journal: European Urology (2022)
Correction:<i>Cliniclal benefit of 1-year certolizumab pegol(CZP) add-on therapy to methotrexate treatment in patients with early rheumatoid arthritiswas observed following CZP discontinuation: 2-year results of the C-OPERA study, a phase III randomised trial</i>
Journal: Annals of the Rheumatic Diseases (2022)

Correction Correction: Cliniclal benefit of 1-year certolizumab pegol(CZP) add-on therapy to methotrexate treatment in patients with early rheumatoid arthritiswas observed following CZP discontinuation: 2-year results of the C-OPERA study, a phase III randomised trial Values are mean ±SD unless otherwise indicated.Data in DB baseline columns represent average during weeks 0-104, whereas data in PT baseline columns represent average during weeks 52-104.*Time from onset of persistent arthritic symptoms.†MTX dose was initiated at 8 mg/week and escalated to the maximum tolerated dose (up to 16 mg/week) by week 8. BMI, body mass index; CCP, cyclic citrullinated peptide; CRP, C reactive protein; CZP, certolizumab pego; DB, double blind; ESR, erythrocyte sedimentation rate; HAQ-DI, Health
Assessment of Predictive Genomic Biomarkers for Response to Cisplatin-based Neoadjuvant Chemotherapy in Bladder Cancer
Authors: Alberto Gil-Jimenez, Jeroen van Dorp, Alberto Contreras-Sanz, Kristan van der Vos, Daniel J. Vis, Linde Braaf, Annegien Broeks, Ron Kerkhoven, Kim E.M. van Kessel, María José Ribal, Antonio Alcaraz, Lodewyk F.A. Wessels, Roland Seiler, Jonathan L. Wright, Lourdes Mengual, Joost Boormans, Bas W.G. van Rhijn, Peter C. Black, Michiel S. van der Heijden
Journal: European Urology (2022)
<i>Notes From the Field:</i> Overdose Deaths Involving Eutylone (Psychoactive Bath Salts) — United States, 2020
Authors: R. Matt Gladden, Vaughne Chavez-Gray, Julie O’Donnell, Bruce A. Goldberger
Journal: MMWR Morbidity and Mortality Weekly Report (2022)

Synthetic cathinones (known as psychoactive bath salts) are a class of potent central nervous stimulants that mimic the effects produced by cocaine, methamphetamine, and methylenedioxymethamphetamine (MDMA; known as ecstasy).Synthetic cathinones have been sold as MDMA (1), distributed as nondrug products (e.g., bath salts) to conceal their sale as an illicit drug and also sold as illicit drug products.*From 2017 to 2021, the supply of eutylone † (a synthetic cathinone) rapidly increased in the United States.During January-June 2017, eutylone was detected in fewer than 10 drug items such as powders, capsules, or tablets obtained through law enforcement activities such as drug seizures, arrests, or undercover buys and tested; during January-June 2021, eutylone was detected in 8,379 drug items, making it the seventh most identified drug during this period (2).Public alerts have been issued and include concern about elevated overdose risk associated with eutylone being sold as MDMA § (1).Little is known about the relative potencies and pharmacological profile of synthetic cathinones compared with MDMA, and using counterfeit tablets potentially increases the risk for overdose; however, additional investigation is needed.CDC, through the State Unintentional Drug Overdose Reporting System (SUDORS), funds 47 states and the District of Columbia ¶ to enhance postmortem toxicology testing and abstract comprehensive data from death certificates and medical examiner or coroner reports, including toxicology reports, for drug overdose deaths of unintentional and undetermined intent.This report describes overdose deaths in which the medical examiner or coroner determined that eutylone contributed to the death (eutylone-involved deaths), submitted
COVID-19 Self-Test Data: Challenges and Opportunities — United States, October 31, 2021–June 11, 2022
Authors: Matthew D. Ritchey, Hannah G. Rosenblum, Kim Del Guercio, Matthew Humbard, Steven Santos, Jason Hall, Jasmine Chaitram, Reynolds M. Salerno
Journal: MMWR Morbidity and Mortality Weekly Report (2022)

Self-tests* to detect current infection with SARS-CoV-2, the virus that causes COVID-19, are valuable tools that guide individual decision-making and risk reduction
<i>QuickStats:</i> Percentage* of Adults† Aged ≥18 Years with Current Hepatitis C Virus Infection,§ by Health Insurance Coverage¶ — National Health and Nutrition Examination Survey, United States, January 2017–March 2020
Journal: MMWR Morbidity and Mortality Weekly Report (2022)

Abbreviation: NHANES = National Health and Nutrition Examination Survey.* With 95% CIs indicated by error bars.† Based on a representative sample of the civilian, noninstitutionalized U.S. population.NHANES data collection was halted in March 2020 because of the COVID-19 pandemic.Data
<i>Notes from the Field:</i> School-Based and Laboratory-Based Reporting of Positive COVID-19 Test Results Among School-Aged Children — New York, September 11, 2021–April 29, 2022
Authors: Eric J. Shircliff, Eli S. Rosenberg, Lauren M. Collens, Dina Hoefer, Emily Lutterloh, Benjamin J. Silk, Amber K. Winn, Travis T. O’Donnell
Journal: MMWR Morbidity and Mortality Weekly Report (2022)

By April 29, 2022, a total of 702,686 COVID-19 cases were reported among children and adolescents aged 5-17 years in the state of New York.*Pediatric COVID-19 cases and hospitalizations increased during the 2021-22 school year, driven by transmission of the Omicron variant † (1).In late 2021, during the surge in Omicron BA.1 variant cases, state § and federal ¶ authorities expanded access to self-administered, at-home rapid antigen tests, which can increase a person's knowledge of their COVID-19 status and guide risk-reduction behaviors.New York government agencies sent millions of these tests to schools for distribution to teachers, students, and staff members.Because results of self-administered, at-home tests are not captured by electronic laboratory reporting (in contrast to health care provider-administered tests at a physician's office or laboratory that are reported through electronic health records or other means), expanded use of these tests might affect interpretation of trends in reported COVID-19 cases; however, this has yet to be assessed** (2).Furthermore, understanding changes in testing behavior before and after the Omicron variant surge might help public health officials better use available COVID-19 data to guide future policy.COVID-19 case data from two independently operating New York State Department of Health systems were compared before and after expansion of at-home testing: 1) laboratoryreported data † † for children and adolescents aged 5-17 years and 2) a kindergarten through grade 12 (K-12) school-based * https://coronavirus.health.ny.